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Abstract

Hepatitis C virus (HCV) elevated expression of the translocase of outer mitochondrial membrane 70 (Tom70). Interestingly, overexpression of Tom70 induces interferon (IFN) synthesis in hepatocytes, and it was impaired by HCV. Here, we addressed the mechanism of this impairment. The HCV NS3/4A protein induced Tom70 expression. The HCV NS3 protein interacted in cells, and cleaved the adapter protein mitochondrial anti-viral signaling (MAVS).Ectopic overexpression of Tom70 could not inhibit this cleavage. As a result, IRF-3phosphorylation was impaired and IFN-β induction was suppressed. These results indicate thatMAVS works upstream of Tom70 and the cleavage of MAVS by HCV NS3 protease suppresses signaling of IFN induction.

Journal

  • Virus Research

    Virus Research 163(1), 405-409, 2012-01

    Elsevier

Keywords

Codes

  • NII Article ID (NAID)
    120004853375
  • Text Lang
    ENG
  • Article Type
    journal article
  • ISSN
    0168-1702
  • Data Source
    IR 
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